- MeSH
- Acetanilides therapeutic use MeSH
- Adrenergic alpha-1 Receptor Agonists pharmacology therapeutic use MeSH
- Muscarinic Antagonists pharmacology therapeutic use MeSH
- Antidepressive Agents, Tricyclic pharmacology therapeutic use MeSH
- Administration, Intravesical MeSH
- Botulinum Toxins, Type A pharmacology MeSH
- Estrogens pharmacology therapeutic use MeSH
- Urinary Bladder, Overactive drug therapy MeSH
- Humans MeSH
- Urinary Incontinence, Stress * drug therapy MeSH
- Thiazoles therapeutic use MeSH
- Urinary Incontinence, Urge * drug therapy MeSH
- Check Tag
- Humans MeSH
- Female MeSH
- MeSH
- Adrenergic alpha-1 Receptor Agonists administration & dosage MeSH
- Ascites drug therapy therapy MeSH
- Adult MeSH
- Hemodynamics drug effects MeSH
- Liver Cirrhosis drug therapy complications physiopathology MeSH
- Kidney physiopathology drug effects MeSH
- Middle Aged MeSH
- Humans MeSH
- Midodrine administration & dosage MeSH
- Pilot Projects MeSH
- Prospective Studies MeSH
- Recurrence MeSH
- Splanchnic Circulation drug effects MeSH
- Vasoconstrictor Agents administration & dosage MeSH
- Treatment Outcome MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Female MeSH
Mesenteric veins are more sensitive than arteries to the constrictor effects of sympathetic nerve stimulation and alpha-adrenoceptor agonists. We tested the hypothesis that alpha(1)- and alpha(2)-adrenoceptors interact to enhance adrenergic reactivity of mesenteric veins. We studied neurogenic and agonist-induced constrictions of mesenteric veins and arteries in vitro. Norepinephrine concentration-response curves were left-shifted in veins compared to arteries. UK 14,304 (0.01-1 microM, alpha(2)-adrenoceptor receptor agonist) did not constrict arteries or veins but enhanced constrictions and Ca(2+) signals mediated by alpha(1)-adrenoceptor stimulation in veins. Yohimbine (alpha(2)-adrenoceptor receptor antagonist) and MK912 (alpha(2C)-adrenoceptor receptor antagonist), but not alpha(2A)- or alpha(2B)-adrenoceptor antagonists, produced rightward shifts in norepinephrine concentration-response curves in veins. Pharmacological studies revealed that alpha(1D)-adrenoceptors mediate venous constrictions. Norepinephrine responses in veins from alpha(2C)-adrenoceptor knock-out (KO) mice were not different from wild type veins. Yohimbine inhibited norepinephrine constrictions in alpha(2C)-adrenoceptor KO veins suggesting that there is upregulation of other alpha(2)-adrenoceptors in alpha(2C)-KO mice. These data indicate that alpha(1D)- and alpha(2C)-adrenoceptors interact in veins but not in arteries. This interaction enhances venous adrenergic reactivity. Mesenteric vein-specific alpha(2)-adrenoceptor linked Ca(2+) and perhaps other signaling pathways account for enhanced venous adrenergic reactivity.
- MeSH
- Adrenergic alpha-1 Receptor Agonists pharmacology MeSH
- Receptors, Adrenergic, alpha-1 metabolism physiology MeSH
- Adrenergic alpha-2 Receptor Agonists pharmacology MeSH
- Adrenergic alpha-2 Receptor Antagonists pharmacology MeSH
- Receptors, Adrenergic, alpha-2 genetics metabolism physiology MeSH
- Mesenteric Arteries drug effects physiology MeSH
- Mice, Inbred C57BL MeSH
- Mice, Knockout MeSH
- Mice MeSH
- Norepinephrine physiology MeSH
- Protein Isoforms antagonists & inhibitors MeSH
- Sympathetic Nervous System drug effects MeSH
- In Vitro Techniques MeSH
- Calcium Signaling drug effects MeSH
- Vasoconstriction drug effects MeSH
- Mesenteric Veins drug effects physiology MeSH
- Dose-Response Relationship, Drug MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Research Support, N.I.H., Extramural MeSH
- Comparative Study MeSH
